Experiments showed that the infection of human CD8+ T lymphocytes with human herpesvirus 6 (HHV-6) resulted in the de novo concomitant expression of CD4. It was also found that HHV-6 infection mediated a down regulation of the CD3 molecule in infected cells, suggesting that HHV-6 may significantly contribute to alterations in the immunocompetence of certain individuals. Additional studies have shown that natural killer cells were susceptible to HHV-6 infection. However, clones of natural killer cells which were reactive with autologous HHV-6 infected lymphocytes were refractory to infection by HHV-6. Following infection of human monocytes, it was found that a proportion of the cells demonstrated increased adherence to endothelial cell monolayers. The increase in adherence did not begin until 48 to 72 hours post-infection. Attempts to identify the ligand responsible for adhesion by flow cytometry were unsuccessful, although the binding was found to be dependent on the presence of divalent cations. Other studies showed that human immunodeficiency virus type 1 (HIV-1) infection promoted the increased expression of tumor necrosis factor but not interleukin 1 nor interleukin 6. The mechanism was shown to be transcriptional activation of the tumor necrosis factor promoter by the viral trans-activator Tat. Additional studies have shown that Tat is released by infected cells soon after infection and is not linked to cell death, suggesting a specific secretory mechanism for the viral protein. Because of the wide variety of effects observed with Tat, additional studies were begun attempting to block the expression of Tat by cells infected with HIV-1. Experiments have shown significant suppression of Tat expression following transfection with antisense ribonucleic acid constructs.